Anyone treating behavioral disturbances in likely CTE cases?

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nowaysanjose

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Thinking of the on-field antics by Antonio Brown yesterday, many people bringing up his concussion in 2015. Anyone taking care of pts like this? I understand you can’t diagnose CTE while living; would it be that dissimilar from treating behavioral issues after TBI?

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I don't know the answer to your question and I'm not a doctor and this is perhaps pedantic, but a concussion is a TBI. I had a psychologist who treated patients with concussions. His advice was a dark room and nothing mentally taxing—I can't remember the period of time. But like a week or so. But from what I recall, just a single concussion was enough to cause neuropsychological changes.

<Again, not a doctor>
 
Compared to the general population, NFL players have a lower incidence of dementia, and a longer life expectancy.

But that doesn't fit the narrative.
 
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Compared to the general population, NFL players have a lower incidence of dementia, and a longer life expectancy.

But that doesn't fit the narrative.

Uh I mean sure compared to the general population considering you're dealing with a subpopulation that is extremely fit and active, literally selected to be paid millions of dollars for their superior athletic abilities. High SE status + best nutrition/doctors in the world + baseline genetic predisposition to be athletic = way higher longer life expectancy baseline.

A better comparison is how they fare vs age matched controls in professional sports with similar earning potential without significant repeated head contact (basketball, baseball, +/- soccer).
 
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I think it's unwise to assume a diagnosis of CTE without ruling out more common diagnoses. In fact, it is unwise to make an armchair diagnosis at all. Behaviorally I have patients with Bipolar I exhibit similar behaviors to Antonio Brown.
 
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I think it's unwise to assume a diagnosis of CTE without ruling out more common diagnoses. In fact, it is unwise to make an armchair diagnosis at all. Behaviorally I have patients with Bipolar I exhibit similar behaviors to Antonio Brown.
Is it really that uncommon in that population though? 110/111 post-mortem brain analyses with CTE findings from the work of Anna McKee in Boston. CTE has been found in the brains of high school athletes as well.
 
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Out of every "CTE" pt that I have been referred, 90%+ have secondary gain and laughably fail PVTs. Most also have extensive histories of substance abuse and/or poorly treated Axis II disorders. These were all 1 or 2 incidence mTBIS. Iatrogenic damage to CTE is by far more damaging than actual head injuries in the mTBI population.
 
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I believe CTE is real, but not common except in people who have had multiple TBIs. It is a novel diagnosis associated with celebrity athletes and therefore an attractive diagnosis for the media and lay people who get fascinated with unusual or bizarre behaviors that they rarely see but psychiatrists see regularly. I'm a little exasperated by it. It's not entertainment. I had a Bipolar patient behave just like Antonio Brown yesterday, but it was slightly less public and not unusual in patients with poor insight. This patient has erected literal billboards but has not made the national news, thankfully.

I treat many combat veterans who have had multiple TBIs, some may also have CTE, if there is a real difference other than cumulative. They usually have comorbid PTSD, Bipolar, substance use disorders, and other more common psychiatric diagnoses, many times predating the TBI. Certainly there is symptomatic overlap with TBI and other diagnoses. I suspect less athletes have PTSD, but other diagnoses likely have similar prevalence.

To answer your original question: At the end of the day, we treat sympomatically. No, treatment is not dissimilar. The VA has done a lot of research and has many resources about treating TBI, you can Google them and search pubmed as well. Research is ongoing but so far not revolutionary in my view from a practical clinical standpoint. Resources and funding are the main limiting factors in caring for irreversible brain damage, as usual. We see this with other forms of dementia daily.
 
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I believe CTE is real, but not common except in people who have had multiple TBIs. It is a novel diagnosis associated with celebrity athletes and therefore an attractive diagnosis for the media and lay people who get fascinated with unusual or bizarre behaviors that they rarely see but psychiatrists see regularly. I'm a little exasperated by it. It's not entertainment. I had a Bipolar patient behave just like Antonio Brown yesterday, but it was slightly less public and not unusual in patients with poor insight. This patient has erected literal billboards but has not made the national news, thankfully.

I treat many combat veterans who have had multiple TBIs, some may also have CTE, if there is a real difference other than cumulative. They usually have comorbid PTSD, Bipolar, substance use disorders, and other more common psychiatric diagnoses, many times predating the TBI. Certainly there is symptomatic overlap with TBI and other diagnoses. I suspect less athletes have PTSD, but other diagnoses likely have similar prevalence.

To answer your original question: At the end of the day, we treat sympomatically. The VA has done a lot of research and has many resources about treating TBI, you can Google them and search pubmed as well. Research is ongoing but so far not revolutionary in my view from a practical clinical standpoint. Resources and funding are the main limiting factors in caring for irreversible brain damage, as usual. We see this with other forms of dementia daily.

At least in my neuro circles, the prevailing thought is also that there is likely a syndrome involved with repetitive head injury. But, that it probably affects individuals who have a predisposition, otherwise some of our larger population studies would look markedly different. Additionally, many of the "hallmarks" of CTE are nonspecific and present in a variety of conditions.

Also, the creep of CTE into people with 1 or 2 isolated, very mild TBIs is exceedingly damaging. Providers usually overlook other factors that explain the pt's sx, and the patients become resistant to psychiatric tx, as everything is due to their "CTE." The cart is well out ahead of the horse on this one.
 
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Uh I mean sure compared to the general population considering you're dealing with a subpopulation that is extremely fit and active, literally selected to be paid millions of dollars for their superior athletic abilities. High SE status + best nutrition/doctors in the world + baseline genetic predisposition to be athletic = way higher longer life expectancy baseline.

A better comparison is how they fare vs age matched controls in professional sports with similar earning potential without significant repeated head contact (basketball, baseball, +/- soccer).


That makes no sense. Either longevity is a problem or it’s not. Except it’s not.

That doesn’t matter because NFL players have a LOWER incidence of dementia than controls. Mcakees pathology findings are better explained by lifestyle factors and other known causes. It’s silly to agtribute a lower incidence of dementia to head injuries in a group that has a lower incidence of dementia than the general population, despite having higher incidences kf known increased risk factors for dementia excluding head injuries. It’s even sillier to think that evolution created a system such as CTE.

Remember, there is objective fraud in the NFL assessments (I.e., see the social masters audit).
 
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That makes no sense. Either longevity is a problem or it’s not. Except it’s not.

That doesn’t matter because NFL players have a LOWER incidence of dementia than controls. Mcakees pathology findings are better explained by lifestyle factors and other known causes. It’s silly to agtribute a lower incidence of dementia to head injuries in a group that has a lower incidence of dementia than the general population, despite having higher incidences kf known increased risk factors for dementia excluding head injuries. It’s even sillier to think that evolution created a system such as CTE.

Remember, there is objective fraud in the NFL assessments (I.e., see the social masters audit).

Wait what? I'm not even sure how this addresses what I'm saying.

I'm saying that comparing professional athletes with a higher incidence of repetitive head trauma to the general population is not the appropriate comparison as that's not really a matched control group for other factors that may influence dementia risk and life expectancy (ex. body weight, nutrition, socioeconomic status, comorbid medical conditions). The appropriate control group would be a control group that is similar in all these other possible confounders except for the repetitive trauma. Saying that they have a lower incidence of dementia and longer life expectancy than the general population total ignores all the confounding variables. You're also ignoring that even grouping "NFL players" into one group probably isn't an appropriate comparison as the risk of head injury varies wildly among various positions (ex. kickers are going to have a much different risk than linemen).

Also, where is the paper that NFL players have a lower incidence of dementia than controls anyway?
 
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Wait what? I'm not even sure how this addresses what I'm saying.

I'm saying that comparing professional athletes with a higher incidence of repetitive head trauma to the general population is not the appropriate comparison as that's not really a matched control group for other factors that may influence dementia risk and life expectancy (ex. body weight, nutrition, socioeconomic status, comorbid medical conditions). The appropriate control group would be a control group that is similar in all these other possible confounders except for the repetitive trauma. Saying that they have a lower incidence of dementia and longer life expectancy than the general population total ignores all the confounding variables.

You're saying that physical prowess prior to 30 years of age (aka, median age of retirement for NFL players) is predictive of the degree of accumulation of p-tau proteins at a median age of 66? Are you aware of data to support that? I'm not.
 
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You're saying that physical prowess prior to 30 years of age (aka, median age of retirement for NFL players) is predictive of the degree of accumulation of p-tau proteins at a median age of 66? Are you aware of data to support that? I'm not.

1) We control for things all the time as possible confounders that don't have definitive evidence as BEING confounders
2) Dementia =/= "p-tau protein accumulation" anyway...take a look back, what you stated was dementia
3) Socioeconomic status and overall physical health are definitely associated with dementia risk...just to name two of the possible confounders I mentioned

this is like a classic strawman argument. None of the confounders I mentioned were "physical prowess prior to 30 years of age".
 
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1) We control for things all the time as possible confounders that don't have definitive evidence as BEING confounders
2) Dementia =/= "p-tau protein accumulation" anyway...take a look back, what you stated was dementia
3) Socioeconomic status and overall physical health are definitely associated with dementia risk...just to name two of the possible confounders I mentioned

this is like a classic strawman argument. None of the confounders I mentioned were "physical prowess prior to 30 years of age".
1) Exactly.
2) Tell that to McAkee and Mez, because they can't get that straight either. The data shows CNS causes of death were limited to 12 individuals, out of 3,439 NFL retirees. Or .03% of NFL retirees. Which is less than 1 additional individual who died from CNS disease than we would expect, based upon national stats. That's all this is.
3) Here's the problem with that. The average age of retirement in the NFL is 27.6 (i.e., prior to 30 years of age). The average age of death for NFL retirees is 57. The average age of the autopsy samples that "confirm CTE" is 66. So unless you are saying that health status at 27.6 is static until death, then physical prowess during the NFL years cannot be considered a confound in the autopsy that confirms CTE at 57 or 66 years of age. Since 78% of NFL players are bankrupt within 2 years of retiring from the NFL, SES is also not a great confound unless it's a strawman.
 
Is it really that uncommon in that population though? 110/111 post-mortem brain analyses with CTE findings from the work of Anna McKee in Boston. CTE has been found in the brains of high school athletes as well.

But even if it's "common" in that population, it doesn't mean all his behaviors can be attributed to it. I have a borderline patient behaving the same way. Sometimes, it's not pathology that drives behavior. Sometimes, people just suck.
 
I believe CTE is real, but not common except in people who have had multiple TBIs. It is a novel diagnosis associated with celebrity athletes and therefore an attractive diagnosis for the media and lay people who get fascinated with unusual or bizarre behaviors that they rarely see but psychiatrists see regularly. I'm a little exasperated by it. It's not entertainment. I had a Bipolar patient behave just like Antonio Brown yesterday, but it was slightly less public and not unusual in patients with poor insight. This patient has erected literal billboards but has not made the national news, thankfully.

I treat many combat veterans who have had multiple TBIs, some may also have CTE, if there is a real difference other than cumulative. They usually have comorbid PTSD, Bipolar, substance use disorders, and other more common psychiatric diagnoses, many times predating the TBI. Certainly there is symptomatic overlap with TBI and other diagnoses. I suspect less athletes have PTSD, but other diagnoses likely have similar prevalence.

To answer your original question: At the end of the day, we treat sympomatically. No, treatment is not dissimilar. The VA has done a lot of research and has many resources about treating TBI, you can Google them and search pubmed as well. Research is ongoing but so far not revolutionary in my view from a practical clinical standpoint. Resources and funding are the main limiting factors in caring for irreversible brain damage, as usual. We see this with other forms of dementia daily.
But certainly you can see the converse also being true, that patients are diagnosed with other more common diagnoses and substance use following prior TBI history where the TBI history is glossed over or ignored completely, right? We are hoping that our history and work ups are adequate but definitely there are times when they are not, no?
 
But certainly you can see the converse also being true, that patients are diagnosed with other more common diagnoses and substance use following prior TBI history where the TBI history is glossed over or ignored completely, right? We are hoping that our history and work ups are adequate but definitely there are times when they are not, no?
Yes, I'm sure it does happen. The good news is like I said - there is no particularly special treatment that I'm not recommending anyway for anyone who has significant cognitive deficits discovered on a thorough examination. Like you noted, we aren't doing autopsies and MRIs are limited in utility. If you are cynical I suppose you could decry the lack of special diagnostic tools and treatments just for CTE alone at this time, but an optimist in every day practice I would say, "hey, even if I miss the diagnosis I'm still treating the symptoms." Which is good because we aren't going to cure CTE but we know what currently helps people with things like TBI and dementia.

If you aren't averse to questionable marketing and practice you could certainly start a CTE clinic, make up a bunch of glossy brochures and a slick website stating how you have specially designed care focusing on CTE (that is actually the standard care for persons with cognitive disorders) and make some money marketing to parents whose kids played Pee Wee football. Strike while the public is still interested in the novelty. Some nice mood lighting, leather upholstery and large windows with a view. Add some essential oils and aroma therapy, get yourself an ex-NFL player to give a testimonial. Offer house calls. People will love it.

I have a separate idea for a fun thread. List all the fads in mental health, things the public loves to champion. My current favorite is Cannabis as a panacea. Maybe "I'm on the autistic spectrum" is #2. I think CTE as a common problem is probably down the list a ways, maybe #20 or so. I'm not sure where psychedelics as a panacea fall, but that's a fun one.
 
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1) Exactly.
2) Tell that to McAkee and Mez, because they can't get that straight either. The data shows CNS causes of death were limited to 12 individuals, out of 3,439 NFL retirees. Or .03% of NFL retirees. Which is less than 1 additional individual who died from CNS disease than we would expect, based upon national stats. That's all this is.
3) Here's the problem with that. The average age of retirement in the NFL is 27.6 (i.e., prior to 30 years of age). The average age of death for NFL retirees is 57. The average age of the autopsy samples that "confirm CTE" is 66. So unless you are saying that health status at 27.6 is static until death, then physical prowess during the NFL years cannot be considered a confound in the autopsy that confirms CTE at 57 or 66 years of age. Since 78% of NFL players are bankrupt within 2 years of retiring from the NFL, SES is also not a great confound unless it's a strawman.

He's not talking about variation in physical prowess during NFL years as a potential predictor of CTE, he is talking about a selection bias introduced by the fact that they are all professional athlete-level healthy at the point they are drafted. Athletic prowess at that level is fairly general (athletes are not infrequently recruited for multiple different sports) and it is a reasonable concern that this might correlate with overall robustness of health generally.

What are the reasons you don't feel that professional athletes in sports with less direct head contact are the appropriate comparison group?
 
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We're a little besides the point, as the "CTE is everywhere" group refuses to examine data of "CTE" in individuals without a known history of TBI or participation in contact sports, which show a similar distribution using their own staging criteria. The only rebuttal I have seen is that "those people must have had TBIs that they were not aware of." When we haven't even established that the C or the T are either necessary nor sufficient to cause the proposed criteria, we have a problem.
 
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We're a little besides the point, as the "CTE is everywhere" group refuses to examine data of "CTE" in individuals without a known history of TBI or participation in contact sports, which show a similar distribution using their own staging criteria. The only rebuttal I have seen is that "those people must have had TBIs that they were not aware of." When we haven't even established that the C or the T are either necessary nor sufficient to cause the proposed criteria, we have a problem.

Yeah, when you get into "well if this finding doesn't match our theory about exposure to Thing X causing Problem Y then they were secretly exposed to Thing X all along!" territory, just stop.
 
Yeah, when you get into "well if this finding doesn't match our theory about exposure to Thing X causing Problem Y then they were secretly exposed to Thing X all along!" territory, just stop.

Seriously, it's like the chronic lyme's people who have never had a bullseye rash, and their titers are zero, but they insist that it's CL because they may have gone for a hike in the woods once.
 
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We're a little besides the point, as the "CTE is everywhere" group refuses to examine data of "CTE" in individuals without a known history of TBI or participation in contact sports, which show a similar distribution using their own staging criteria. The only rebuttal I have seen is that "those people must have had TBIs that they were not aware of." When we haven't even established that the C or the T are either necessary nor sufficient to cause the proposed criteria, we have a problem.
I read an article on subdural hematomas, and there really were people who did not remember their minor head injuries that caused the hematomas:

People have all sorts of exposures all the time, and you know the saying that every egg cracks differently.

People didn't believe until recently that pain during early infancy caused long-term effects (or even whether infants could feel pain), and now it's widely recognized that painful experiences as an infant do have long-term effects. It doesn't mean that it will affect everyone the same or universally. But I don't think we can say that insults and injuries universally have no effect and that the effects won't be heterogeneous.
 
I read an article on subdural hematomas, and there really were people who did not remember their minor head injuries that caused the hematomas:

People have all sorts of exposures all the time, and you know the saying that every egg cracks differently.

People didn't believe until recently that pain during early infancy caused long-term effects (or even whether infants could feel pain), and now it's widely recognized that painful experiences as an infant do have long-term effects. It doesn't mean that it will affect everyone the same or universally. But I don't think we can say that insults and injuries universally have no effect and that the effects won't be heterogeneous.

You can get SDHs without a blow to the head. Also, you're still only looking at the T part, and pretty much only in an elderly population. What you are implying is that a fairly large number of people, most of whom are not elderly, who have many TBIs of which they have no knowledge of ever having experienced. If we follow this to a logical conclusion, we are all at risk for CTE from events so minor as to include accidentally bumping into a door or putting on a hat too forcefully.
 
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I read an article on subdural hematomas, and there really were people who did not remember their minor head injuries that caused the hematomas:

People have all sorts of exposures all the time, and you know the saying that every egg cracks differently.

People didn't believe until recently that pain during early infancy caused long-term effects (or even whether infants could feel pain), and now it's widely recognized that painful experiences as an infant do have long-term effects. It doesn't mean that it will affect everyone the same or universally. But I don't think we can say that insults and injuries universally have no effect and that the effects won't be heterogeneous.
I wouldn't be surprised if medical problems in infancy can have long term medical or neurologic consequences, but I am unaware of credible research that supports that infants who have had pain have subsequent psychiatric illness caused by that pain. I am skeptical. I am forcefully putting on my skeptic hat and hoping I don't get CTE.
 
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I wouldn't be surprised if medical problems in infancy can have long term medical or neurologic consequences, but I am unaware of credible research that supports that infants who have had pain have subsequent psychiatric illness caused by that pain. I am skeptical. I am forcefully putting on my skeptic hat and hoping I don't get CTE.
It's funny you mention hat—I actually wore a bike helmet when being driven in cars as a child. Chalk that up to my neurotic temperament.

It's a very controversial topic when I bring it up, but there was a Danish study that did link early infant circumcision to long-term mental health outcomes, and it was consistent even when accounting for cultural background, which many would assume was the cause. Countries like Denmark are perfect for that type of research because they have national health registries that can look at this type of data longitudinally. Unfortunately, due to various international pressures, they were forced to abandon that particular database. But early infant circumcision in US studies had already been linked to higher pain responses at subsequent vaccinations. The Danish study went further, and I'm not saying the data shouldn't be further explored and that it is conclusive--unfortunately though it is too controversial for people to continue studying and valuable databases were destroyed. It's a whole fracas when I bring up the disorders it was linked to, due to earlier specious claims made about vaccines, which I do not believe are credible.
 
It's funny you mention hat—I actually wore a bike helmet when being driven in cars as a child. Chalk that up to my neurotic temperament.

It's a very controversial topic when I bring it up, but there was a Danish study that did link early infant circumcision to long-term mental health outcomes, and it was consistent even when accounting for cultural background, which many would assume was the cause. Countries like Denmark are perfect for that type of research because they have national health registries that can look at this type of data longitudinally. Unfortunately, due to various international pressures, they were forced to abandon that particular database. But early infant circumcision in US studies had already been linked to higher pain responses at subsequent vaccinations. The Danish study went further, and I'm not saying the data shouldn't be further explored and that it is conclusive--unfortunately though it is too controversial for people to continue studying and valuable databases were destroyed. It's a whole fracas when I bring up the disorders it was linked to, due to earlier specious claims made about vaccines, which I do not believe are credible.

This is actually a weird area that I have some knowledge of the research in as my spouse does circumcisions as an aspect of her work. Of the actual comprehensive research, meta-analyses do not show any sexual health differences between those who have this done as infants and those who do not. There's some very low n research about people who get it done later in life, but the data is not compelling or us vastly underpowered. If you have any data about later psychiatric issues aside from the retracted Danish study, I'd love to look at it.
 
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This is actually a weird area that I have some knowledge of the research in as my spouse does circumcisions as an aspect of her work. Of the actual comprehensive research, meta-analyses do not show any sexual health differences between those who have this done as infants and those who do not. There's some very low n research about people who get it done later in life, but the data is not compelling or us vastly underpowered. If you have any data about later psychiatric issues aside from the retracted Danish study, I'd love to look at it.
It was very long ago that I read about this, and I don't believe it was ever retracted—it was just that the database Denmark kept was destroyed based on other countries (trying to avoid geopolitics) saying they shouldn't be keeping that type of data. Just googling quickly this is what I came across:


If you want to know more about the subject, Brian Earp is the one to look up. He's written very extensively on all of the various research and synthesized and analyzed it.
 
It was very long ago that I read about this, and I don't believe it was ever retracted—it was just that the database Denmark kept was destroyed based on other countries (trying to avoid geopolitics) saying they shouldn't be keeping that type of data. Just googling quickly this is what I came across:


If you want to know more about the subject, Brian Earp is the one to look up. He's written very extensively on all of the various research and synthesized and analyzed it.

Ah, I've actually seen that one, it has some methodological limitations. Has this research ever been replicated in another comprehensive study. Also, Earp is a known "crusader" in this area.


 
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Ah, I've actually seen that one, it has some methodological limitations. Has this research ever been replicated in another comprehensive study. Also, Earp is a known "crusader" in this area.


No, I don't know of it being replicated with regard to defined illnesses, but I have read other studies that link it to higher pain responses in vaccinations six months post-circumcision. And as I said, I think it's probably something that is difficult to do with various pressures against studying it and that most countries wouldn't have the type of databases that Denmark did. When it's a medical procedure that's sought out for non-medical reasons or even when people believe it is necessary for their very existence (which was one of the arguments for the destroying the data as they thought having the data itself was a slippery slope), there aren't going to be a lot of people who are going to be enthusiastic about finding downsides to it.

Brian Morris has quite a reputation of his own. He's not only a crusader, but has written songs and poetry in favor of circumcision and some rather . . . bizarre enthusiasm and various front groups that are at best a bit unsavory.
 
No, I don't know of it being replicated with regard to defined illnesses, but I have read other studies that link it to higher pain responses in vaccinations six months post-circumcision. And as I said, I think it's probably something that is difficult to do with various pressures against studying it and that most countries wouldn't have the type of databases that Denmark did. When it's a medical procedure that's sought out for non-medical reasons or even when people believe it is necessary for their very existence (which was one of the arguments for the destroying the data as they thought having the data itself was a slippery slope), there aren't going to be a lot of people who are going to be enthusiastic about finding downsides to it.

Brian Morris has quite a reputation of his own. He's not only a crusader, but has written songs and poetry in favor of circumcision and some rather . . . bizarre enthusiasm and various front groups that are at best a bit unsavory.

Back to @wolfvgang22 question, though, it does not appear that there is compelling evidence at the moment to support this claim as of yet. What does exist is deeply flawed, and there is no independent replication of that flawed research.
 
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He's not talking about variation in physical prowess during NFL years as a potential predictor of CTE, he is talking about a selection bias introduced by the fact that they are all professional athlete-level healthy at the point they are drafted. Athletic prowess at that level is fairly general (athletes are not infrequently recruited for multiple different sports) and it is a reasonable concern that this might correlate with overall robustness of health generally.

What are the reasons you don't feel that professional athletes in sports with less direct head contact are the appropriate comparison group?
The only way they’ve diagnosed CTE is through autopsy. The dead guys median age is between 57-66. That is about 3 decades after they retired.

I have no issue with saying they were healthy while they were playing. But not when they died.

They’ve done studies about low victory vs high velocity NFL player. But the metric changes from “died due to CNS disease” to “CNS disease was a secondary CPT code at time of death”. That’s disingenuous.

By a pure numbers game, you’d think NFL careers were more associated with cancer than dementia. But the financial incentive is in dementia. In a population that is known to go broke, and have a very clear documented history of lying about cognitive problems.
 
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The only way they’ve diagnosed CTE is through autopsy. The dead guys median age is between 57-66. That is about 3 decades after they retired.

I have no issue with saying they were healthy while they were playing. But not when they died.

They’ve done studies about low victory vs high velocity NFL player. But the metric changes from “died due to CNS disease” to “CNS disease was a secondary CPT code at time of death”. That’s disingenuous.

By a pure numbers game, you’d think NFL careers were more associated with cancer than dementia. But the financial incentive is in dementia. In a population that is known to go broke, and have a very clear documented history of lying about cognitive problems.

And, at least for players who played through the 70s through early 90s frequent and generally team supplied opioids and amphetamines.
 
I do deal with severe TBIs on inpatient sometimes, but CTE...no.
 
This is a great discussion. CTE is a post-mortem diagnosis and you shouldn't make it in the living, but that doesn't stop neurologists from making the diagnosis in their clinics. The National Institute of Neurological Disorders and Stroke (NINDS) set an initial research diagnostic criteria for a Traumatic Encephalopathy Syndrome (TES) in 2014 that included cognitive symptoms, mood/behavioral, and motor symptoms. It showed really good sensitivity and interrater reliability but had poor specificity (good rule out but not a great rule in for CTE). Actually, the mood/behavioral and motor symptoms were pretty poor predictors because there was often a high baseline rate of these in the general population anyways and cognitive symptoms were the most specific of them.

The new criteria for TES that came out last year (2021) from the NINDS include four criteria: repetitive head trauma; clinical features of cognitive impairment (episodic memory and/or executive function, should be based on neuropsychological evaluation) and/or neurobehavioural dysregulation (they defined this as explosive behavior, anger, impulsivity, but largely is subjective); a progressive course of disease (which is debated because CTE being neurodegenerative is far from proven); and clinical features not fully accounted for by another condition. This is meant to be a research diagnosis and NOT meant to be made in clinical practice yet.

There's actually a nocebo effect that has been demonstrated in people who get diagnosed with CTE, who end up having a worse prognosis when they don't actually meet criteria for this postmortem, so I would really caution making this diagnosis or going along with it in clinical practice. This nocebo effect extends to "postconcussive syndrome" and "second impact syndrome" and even just plain old "concussion."
 
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It showed really good sensitivity and interrater reliability but had poor specificity (good rule in but not a great rule out for CTE).

One of those things should probably be the opposite 😉(idk which one it is cause I don’t know if that criteria has better sensitivity or specificity). If I had to guess I’d guess good NPV but not good PPV (which aren’t the same thing of course but I think that’s what you’re getting at).
 
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This nocebo effect extends to "postconcussive syndrome" and "second impact syndrome" and even just plain old "concussion."
What differentiates CTE from PPCS? Progressive decline (despite controversy) and multiple TBI's?

I have had a few patients in the past year who presented for reported issues since TBI. Some mood, some cognitive. Is this more controversial than I had thought somehow?
 
What differentiates CTE from PPCS? Progressive decline (despite controversy) and multiple TBI's?

I have had a few patients in the past year who presented for reported issues since TBI. Some mood, some cognitive. Is this more controversial than I had thought somehow?

Need a few rule outs for both. 1. Are they in litigation related to the alleged TBI? 2. Are they currently enrolled in a TBI clinic that is likely iatrogenic. 3. Are they prone to somaticization? Caveat, this is regarding uncomplicated mTBI.
 
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High sensitivity good for ruling out

High specificity good for ruling in

I’m sure @clozareal already knows this. Rest of his post suggests so
yeah sorry this is what i meant
 
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What differentiates CTE from PPCS? Progressive decline (despite controversy) and multiple TBI's?

I have had a few patients in the past year who presented for reported issues since TBI. Some mood, some cognitive. Is this more controversial than I had thought somehow?

CTE is a postmortem neuropathological whereas postconcussive syndrome is a clinical one (although has no consensus criteria). Not everyone who has PPCS, SIS, or repetitive head trauma will have CTE. No consensus on what the minimum threshold is yet and even between two people who have similar amounts of exposure, it's not clear why one may develop CTE and the other may not.

TES captures postconcussive syndrome and repetitive MTBI as part of the criteria.

Mood, cognitive, anxiety, insomnia, and personality changes can all happen after a TBI. The only change in management is that you'll need to go lower and slower on your titration of medications you'd normally use for it. Some of the main exceptions is pathological laughter/crying (pseudobulbar affect) which has some FDA approved treatments (Nuedexta), and a few lower evidence-based but used methods: methylphenidate for combative behavior, beta-blockers for agitation/aggression, amantadine for irritability.
 
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Thinking of the on-field antics by Antonio Brown yesterday, many people bringing up his concussion in 2015. Anyone taking care of pts like this? I understand you can’t diagnose CTE while living; would it be that dissimilar from treating behavioral issues after TBI?
Just my 0.02, AB seems more like narcissistic personality d/o than anything else...of all the people getting wacked in the head any given Sunday why does this one (very very talented) person get the CTE question

I have treated TBI, antisocial, Intellec disability, Borderline, manic, and general Impulse Control d/o patients and after a while its easier to see what's driving the behavior ...no CTE patients but AB definitely checks off a lot in the narcissistic PD category....far more than the TBI patients
 
Just my 0.02, AB seems more like narcissistic personality d/o than anything else...of all the people getting wacked in the head any given Sunday why does this one (very very talented) person get the CTE question

I have treated TBI, antisocial, Intellec disability, Borderline, manic, and general Impulse Control d/o patients and after a while its easier to see what's driving the behavior ...no CTE patients but AB definitely checks off a lot in the narcissistic PD category....far more than the TBI patients

Also, dude had behavior issues, though not to the recent level, back in his college days. Unfortunately, we see people gripped by the "good ole days" delusion with mTBI all of the time when the medical records clearly show otherwise.
 
Decided to browse the Psychiatry forum and saw this thread. Sorry, if I’m a bit of a Johnny-Come-Lately.

I taught an introductory neuro basis of behavior class last semester and looked into this topic. Obviously, not well versed in this area and really appreciate some of the information and debate about the evidence. My biggest concerns were as follows and any counterpoints on the topic are appreciated.

1. The post mortem studies are highly flawed since they provide a very biased selection of brains.

2. Generally speaking, after a physical injury to the brain time tends to heal or reduce cognitive/neurological problems. However, this putative disorder gets worse over the next few decades. Meaning, it’s hard to believe that repeated concussion lead to a worse problem 30 years later.

3. Seemingly, many better alternate theories to these problems than CTE (confounds such as drug or steroid use, behavioral learning for suicide and explosive behavior in athletes that experience very different contingencies than the average person).

4. This is a small reason and not related to the data but more about the history of CTE. The guy that first popularized CTE (Will Smith in the movie) has stopped doing anything related to science and makes a living selling the idea of CTE.

The student athletes are very interested in this topic and the textbooks are very sparse on the topic (unsurprisingly). I’d like to be a bit more informed on the subject.
 
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Decided to browse the Psychiatry forum and saw this thread. Sorry, if I’m a bit of a Johnny-Come-Lately.

I taught an introductory neuro basis of behavior class last semester and looked into this topic. Obviously, not well versed in this area and really appreciate some of the information and debate about the evidence. My biggest concerns were as follows and any counterpoints on the topic are appreciated.

1. The post mortem studies are highly flawed since they provide a very biased selection of brains.

2. Generally speaking, after a physical injury to the brain time tends to heal or reduce cognitive/neurological problems. However, this putative disorder gets worse over the next few decades. Meaning, it’s hard to believe that repeated concussion lead to a worse problem 30 years later.

3. Seemingly, many better alternate theories to these problems than CTE (confounds such as drug or steroid use, behavioral learning for suicide and explosive behavior in athletes that experience very different contingencies than the average person).

4. This is a small reason and not related to the data but more about the history of CTE. The guy that first popularized CTE (Will Smith in the movie) has stopped doing anything related to science and makes a living selling the idea of CTE.

The student athletes are very interested in this topic and the textbooks are very sparse on the topic (unsurprisingly). I’d like to be a bit more informed on the subject.

Just a quick point to this one, retired NFL players actually have significantly lower rates of suicide compared to the general population, Iverson and others have looked at this in large NFL samples. People just think it's higher because when it does happen it is HIGHLY publicized and the CTE cults shout it loud and proud.
 
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Just a quick point to this one, retired NFL players actually have significantly lower rates of suicide compared to the general population, Iverson and others have looked at this in large NFL samples. People just think it's higher because when it does happen it is HIGHLY publicized and the CTE cults shout it loud and proud.

I worked once with a former NFL player who did have a couple of nasty sounding concussions with transient neurological symptoms but years later developed sensorimotor OCD that was kind of triggered by his worries about CTE. Stuff like "am I breathing correctly? how about now? how about now? What if my head trauma means I'll never breathe correctly? What if the fact I can't sleep isn't because I'm obsessing about my breathing is actually because of my head trauma and I'll never sleep again?", constantly seeking reassurance about his breathing from friends and family, etc. etc. Had moved on to a second career that was pretty cognitively demanding and doing well for himself, but it was this, years later, that crippled him for a while.
 
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I worked once with a former NFL player who did have a couple of nasty sounding concussions with transient neurological symptoms but years later developed sensorimotor OCD that was kind of triggered by his worries about CTE. Stuff like "am I breathing correctly? how about now? how about now? What if my head trauma means I'll never breathe correctly? What if the fact I can't sleep isn't because I'm obsessing about my breathing is actually because of my head trauma and I'll never sleep again?", constantly seeking reassurance about his breathing from friends and family, etc. etc. Had moved on to a second career that was pretty cognitively demanding and doing well for himself, but it was this, years later, that crippled him for a while.

The nocebo/iatrogenic effect is real and potentially devastating here. The number of people who think that they have a devastating and irreversible degenerative condition is likely exponentially higher than the people who do likely have a degenerative condition that is a consequence of head trauma.
 
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IIRC, my last review of the prevalence of CTE in NFL players was really low, in the single digit percentage or maybe low teens even thought hey had the same amount of exposure to multiple head traumas. This is the danger in making a diagnosis of a postmortem condition while someone is still alive. The nocebo effect is extremely damaging and a clinical diagnosis of CTE/TES should not be made at this time unless you're part of a research setting.
 
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